Currently, the literature features controversial reports on the relationship between SUA and cerebral infarction. Many studies have found elevated SUA indicative of a poor prognosis (dead or be in care) in vascular event , especially elevated SUA increasing the incidence of myocardial infarction and chronic renal failure . Furthermore, large cohort studies have also shown that SUA is an important independent risk factor for cardiovascular mortality and SUA may increase the risk of cardiovascular events? [4, 16–19].
Chamorro et al confirmed that patients with good prognosis had higher SUA levels in the acute stage of cerebral infarction classically . In this study, the results showed that young cerebral infarction patients with better prognosis had elevated levels of SUA on admission, and that patients within the lowest quintile of SUA levels suffered from severer dysfunctions compared with those patients within the highest quintile.
Waring et al also demonstrated that SUA reduced exercise-induced oxidative stress in healthy adults. In this study, we also compared SUA levels between age and gender-matched control population, and young patients with cerebral infarction, and found SUA concentrations in healthy controls is higher than in cerebral infarction patients.
In our study, we demonstrated that the worst prognosis was related with the lowest admission SUA levels in cardiogenic cerebral infarction patients. thus, patients with cerebral infarction caused by blockage of small blood vessels had the better prognosis and higher SUA levels on admission, which further illustrates that high SUA level on admission is helpful for functional recovery in young cerebral infarction patients.
In patients with acute stroke, the SUA concentrations decreases significantly over time, and their plasma antioxidant capacity is inversely related to the volume of cerebral infarction and the severity of neurological impairment . Neurological impairment at stroke onset and final infarction size at follow-up are inversely related with the concentration of SUA . Although the SUA level at stroke onset is associated with the presence and duration of atherosclerotic risk factors and the severity of atherosclerotic disease, the odds of good clinical outcome after the ischemic insult increases 12% for each milligram per deciliter increase of SUA . Our study further suggests that SUA confers significant protection as an antioxidant and anti-free radical in young acute cerebral infarction patients, ant that SUA administration may become a new target for neuroprotection in cerebral infarction patients. Waring et al had administrated the UA in healthy control and observed a significant increase in the free-radical scavenging capacity of serum, using two methodologically distinct antioxidant assays. The effect of SUA was substantially greater than that of vitamin C .
Why is SUA generally lower in the cerebral infarction patients with poor prognosis? Experimental data can provide some understanding to these findings from several ways: first, ischemic neuronal damage studies have shown that addition of physiological concentrations of UA protects hypothalamic neurons from excitotoxic and metabolic injury in vitro ; second, normal SUA concentrations in human plasma was able to almost completely prevent the inactivation of SOD3 by H2O2. Some studies indicate that local SUA concentrations increase during acute ischemic events, which might be a compensatory mechanism that inhibited the increase of free radical activity ; thirdly, the elevated SUA concentrations also reduce oxidative stress caused by acute physical exercise, as reflected by plasma 8-iso-PGF2αconcentrations . In our studies, we also found that higher admission platelet concentration resulted in better prognosis. This discovery is very significant, however, because this was not the main aim of the study, we cannot exclude the prognostic influence of these factors. In our future work, we will focus on more meaningful clinical indicators.
With regards to the time of SUA quantification, we made reference to the measurement of Chamorro A et al ; we measured the SUA on admission in order to avoid any interference by the intensity of fluid replacement or the heterogeneous administration of medical therapies.
In our analysis, the interfering factors such as creatinine levels, electrolyte levels, and the factor of with or without kidney disease were considered. All selected patients were admitted to hospital within 72 hours in order to remove the impact of time of onset as well as bed rest on the SUA level.
However, two limitations existed which should be taken into account when assessing the results. First, subgroup analysis has been limited by the relatively small sample size, which might also have caused the non-significance of some statistical tests. Second, these patients were not followed up, so that the long-term prognostic significance of early SUA measurements could not be documented, although not included among the goals at the onset of this investigation.